One of the most complex clinical problems in obstetrics and neonatology is caring for pregnant women at the threshold of viability. Births near viability boundaries are grave events that carry a high prevalence of neonatal death or an increased potential for severe lifelong complications and disabilities among those who survive. Compared with several decades ago, premature infants receiving neonatal care by today's standards have better outcomes than those born in other eras. However, preterm labor at periviability represents a more complex counseling and management challenge. Although preterm birth incidence between 20/7 and 25/7 weeks has remained unchanged, survival rates at earlier gestational ages have increased as perinatal and neonatal specialties have become more adept at caring for this at-risk population. Women face difficult choices about obstetric and neonatal interventions in light of uncertainties around survival and outcomes. This article reviews current neonatal statistics in reference to short- and long-term outcomes, key concepts in obstetric clinical management of an anticipated periviable birth, and counseling guidance to ensure shared-decision making.Offspring born preterm (ie, before 37 weeks of gestation) are more likely to die or experience long-standing illness than full-term offspring. Maternal genetic variants (ie, heritable, stable variations in the genetic code) and epigenetic modifications (ie, chemical modifications to the genetic code that can affect which genes are turned on or off) in response to stress have been implicated in preterm birth. Fetal genetic variants have been linked to preterm birth though the role of offspring epigenetics in preterm birth remains understudied. This systematic review synthesizes the literature examining associations among stress during pregnancy and epigenetic modifications to offspring DNA, with 25 reports identified. Ten reports examined DNA methylation (ie, addition/removal of methyl groups to/from DNA) across the epigenome. The remainder examined DNA methylation near genes of interest, primarily genes linked to hypothalamic-pituitary-adrenal axis function (NR3C1, FKBP51), growth/immune function (IGF2), and socioemotional regulation (SLC6A4, OXTR). The majority of reports noted associations among stress and offspring DNA methylation, primarily when perceived stress, anxiety, or depression served as the predictor. Findings suggest that differences in offspring epigenetic patterns may play a role in stress-associated preterm birth and serve as targets for novel interventions.This qualitative grounded theory pilot study investigated the concerns and coping mechanisms of mothers of very low-birth-weight (VLBW; less then 1500 g) infants following discharge from the neonatal intensive care unit in Alberta, Canada. In-depth, semistructured, face-to-face, audio-recorded interviews were conducted with women of VLBW infants. Interviews lasting 75 to 90 minutes were transcribed verbatim and coded using grounded theory methodology. Data saturation and theoretical redundancy were achieved in interviews with 6 mothers of VLBW infants. The core variable of "reconstructing normal" emerged from the interview data. Women indicated that mothering a VLBW infant is an unfolding experience that is continuously being revised, creating a new sense of normal. The construct consists of 4 categories; mother-infant relationship, maternal development, maternal caregiving and role-reclaiming strategies, and infant developmental milestones. Findings from this study suggest that women found the transition into motherhood following the birth of a VLBW infant as a multidimensional and dynamic process. Further research is warranted to confirm these results and to further explore mothering issues with VLBW infants.Preterm birth remains a leading cause of morbidity and mortality during the perinatal and neonatal periods. Now affecting approximately 1 in 10 births in the United States, preterm birth often occurs spontaneously and without a clear etiology. Careful assessment of risk factors, however, identifies vulnerable women allowing targeted interventions such as progestogen therapy and cerclage. This article is intended to highlight preterm birth risk factors and current predictive and preventive strategies for midwives, nurse practitioners, clinical nurse specialists, and perinatal nurses.PURPOSE OF REVIEW To critically appraise new insights into the biology of remnant lipoproteins and their putative role in the pathophysiology of atherosclerotic cardiovascular disease, and to compare the atherogenicity of remnant particles with that of low-density lipoproteins (LDL). RECENT FINDINGS New in-vivo stable isotope tracer studies of the kinetics of apoB48 and apoB100-containing lipoproteins in postprandial conditions have revealed that apoB48-containing very low-density lipoproteins (VLDL) accumulated markedly in hypertriglyceridemic patients. These intestinally-derived particles were cleared slowly, and represented up to 25% of circulating VLDL; as part of the remnant particle population, they may increase cardiovascular risk. Importantly, the PCSK9 inhibitor, evolocumab, was shown to reduce remnant levels (-29%) during the postprandial period in diabetic patients on statin therapy - an effect which may be additive to that of LDL-cholesterol reduction in conferring cardiovascular benefit. In recent Mendelian randomization studies, the effect of lowering triglyceride-rich lipoproteins or LDL-cholesterol translated to similar clinical benefit per unit of apoB. Finally, in randomized trials involving statin-treated patients with atherosclerotic cardiovascular disease, remnant cholesterol levels were associated with coronary atheroma progression independently of LDL-cholesterol. https://www.selleckchem.com/products/oligomycin-a.html SUMMARY Overall, data from observational studies in large cohorts, Mendelian randomization studies, meta-regression analyses, and post-hoc analyses of randomized trials are consistent with the contention that remnants are highly atherogenic particles and contribute to the atherosclerotic burden in an equivalent manner to that of LDL.